Thrombosis Flashcards
Thrombus thrombosis
Solidification of blood contents forms within vascular system during life
Thrombosis is how it is formed
What can cause thrombosis
Virchows triad
Abnormal blood flow
Hypercoagulability
Endothelial injury
Endothelial injury
Formation thrombi in heart and arteries
At sites of MI
ulcerated plaques in atherosclerosis
Injured endocardium
Valves with inflammatory valve disease and prosthetic valves
Radiation chemical bacteria immunological do plastic
Platelets role
Platelet undergo 3 important reactions after injury
Adhesion
Secretion
Aggregation
Pathogenesis endothelial injury
Vasoconstriction - endothelin
Hemostasis - ADP, TXA, Pf4, vWF Platelets adhesion Shape change Granule release ADO TXA2 Recruitment Aggregation
Secondary hemostasis
Tissue factor, release of phospholipid complex expression, thrombin activation, fibrin polymerisation
Thrombus and antithrombotix events
Release tPA and thrombomodulin
Trapped blood cells and neutrophils
Deficiency of Gpllblla
Glanzmanns theombasthenia
Defiency od Gplb
Bernard doilies syndrome
Deficiency of Von willebrand factoe
Von willbrand disease
Alterations in normal blood flow
Tuberulence contributes to development of arterial and cardiac thrombi
Stasis contributes to venous thrombosis
Turbulence and stasis
Disrupt laminar flow
Prevent dilution of coagulation factors
Stop clotting factor inhibitors
Promote endothelial cell activation
Hypercoagulability
Alteration of blood coagulation mechanism which predisposes thrombosis
Primary genetic - mutation v gene leiden mutation, antithrombin deficieny lll, protein c and sndeficiency
Secondary acquired - high risk bed rest immobilisation, tissue damage prosthetic valves DIC smoking sickle cell anaemia
Morphology of thrombi
Mural thrombi
Arterial thrombi
Venous thrombosis
Mural thrombi
Applied to one wall of underlying structure
Occurs in capacious lumina of Heart chambers and aorta
Arterial thrombosis
In coronary arteries, cerebral and femoral arteries
Thrombi hydrology
Laminations called lines of Zahn
Pale band is fibrin and platelets
Red band is RBCs
Venous thrombosis
Occlusive dark red
Affect veins of lower legs 90
Deep calf femoral popliteal iliac veins
Thrombophlebitis- inflamed and thrombosis
Fate of thrombus
Resolution
Lungs
Organised and incorporated into wall
Organised and recanalisdd
Arterial thrombosis
Loss of pulses distal to thrombus
Area is cold pale painful oaraesthesia
Tissue dies and gangrene
Venous thrombosis can be
Superficial saphenouscongrstion swelling pain tender (rarely embolise)
Deep foot and ankle odemea
Homans sign
Asymptomatic
Treatment
Stockings
Anticoagulant drugs
Herpain IV and warfarin ORAL
Embolus
Detached solid that is carried by blood to distant site
90% all emoji arise in thrombus
Embolism
Bone bone marrow Atheromatus debris Droplets of fat Tumor Foreign bodies bullet Sbublles of air nitrogen
Pulmonary embolism
Occlusion of large pulmaonry artery
95 due to thrombinin veins of lower leg
May impact main pulmonary artery or lodge at bifurcation as saddle emobilus
Consequences of pulmonary embolism
Respiratory compromise
Haemodynamic comprosmise
LARGE PENinstatenous death
Pulseless electrical activity PEA
Smaller pe cause
Acute respiratory and cardiac problems
Systemic embolism
through arterial circulation
Arise form thrombi in heart
Ulcerated atherosclerotic plaque
Aortic aneurysm
Infective endocarditis
Valvular or aortic prosthesis
Cause infarction
Lower extremities, brain, viscera, upper limbs
Air embolism
Bubbles in circulation obstruct vascular flow and damage tissues
Barotruma
Delivery or abortion
Pneumothorax
Injury chest wall
Caisson disease or decompression sickness
What’s caisson diseas
Scuba deep sea workers in underwater individual decompressed too rapidly, helium and nitrogen form gaseous emboli
Treatment for caisson disease
Decompression chamber
Fat embolism
Minute globules of fat - fracture of shafts and soft tissue trauma
Fat embolism syndrome
Fat embolism pathogenesis
Mechanical - microagreagtes of neutral fat cause occlusion
Chemical - free fatty acids release from fat globules result in toxic injury to vascular endothelium
Detecting dat embolism
Pulmonary insufficnxy
Neurological symptoms
Anaemia and thrombocytopenia
Latent after 24/72 hrs
Amniotic fluid embolism
Rare labour maternal mortality 86%
Caused by infusion of amniotic fluid into maternal circulation
Respiratory difficulty
Convulsions
Coma
Infarct
Area of ishcaemic necrosis caused by occlusion of arterial supply or venous drainage of tissue
Causes of infarcts
99%
Thrombosis
Embolism
Types of infarcts
Red haemorrhagic
Venous occlusion in loos tissues and in tissue wth dual circulation
White anaemia
Arterial occlusion in solid organs
Septic or bland
Infarcts in ovary
Venous occlusion dark blue and haemorhiagic
Lung infarction
Loose tissue wedge red and haemorjiax
Small intestine infarct
Dual circulation
Red and haemorrhagic
Histology of infarction
Ischaemic coagulative necrosis mins to days (liquefaction in CNS)
Inflammation response house - 7 days
Reparative response (1-2 wks)
Scaring (2wks to 2 months)
